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6 publications mentioning hsa-mir-1912

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-1912. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 60
For hsa-miR-1912 an upregulated miRNA expression using all three apoptosis inductors was observed. [score:6]
This is in line with previous data showing that the expression of miR-147b and miR-1912 is also downregulated in other kinds of cancer tissues like breast cancer or non-small cell lung cancer compared to non-cancerous tissue [68, 69]. [score:5]
Hence we analyzed the basal expression of both strands of the three human miRNAs miR-96, miR-1912 and miR-147b in S KOV3 cells and observed an upregulation of both mature hsa-miR-96 strands in S KOV3 cells compared to the non-cancerous cell line SGBS. [score:5]
After ectopic introduction of miR-96, miR-1912 and miR-147b we detected an enhanced expression of pro-apoptotic proteins Bak1 and Bax for all miRNAs except the mouse-specific miR-3073a, which only showed elevated expression of Bax (Figure 6A). [score:5]
The analysis of basal expression of specific pro-apoptotic miRNAs miR-147b and miR-1912 in the ovarian cancer cells compared to non-cancerous SGBS cells demonstrated a reduced expression in ovarian cancer cell lines. [score:4]
Additive effects of miR-1912-5p, -147b-5p, -96-5p or -3073a-3p in combination with carboplatin in S KOV3, OVCAR3, TOV21G, TOV112D, A2780 and even in the cisplatin resistant cell line A2780-cis suggest a potential benefit in combined application behind the recent treatment with established VEGF -inhibitors. [score:3]
Of these miR-1912, miR-147b and miR-93 are expressed in human tissues while miR-682 was found to be mouse specific (miRBase Version 21). [score:3]
Effects of apoptosis inducers on the expression of mature hsa-miR-96 (C), hsa-miR-147b (B) and hsa-miR-1912 (D) in S KOV3 cells. [score:3]
With respect to the p53 state of the ovarian cancer cell lines with different genetic background harboring either wildtype (TOV21G, A2780) or functionally mutated p53 (OVCAR3 [p53R248Q], TOV112D [p53R175H], A2780-cis [p53K351N]), or even lacking p53 expression (S KOV3) the strong pro-apoptotic effects observed in the recent study might suggest a potential p53-independent mode of action of miR-1912-5p, -147b-5p, -96-5p and -3073a-3p that offers the opportunity to overcome p53 dependent treatment resistance. [score:3]
The highest upregulation of the hsa-miR-1912 level was measured after etoposide treatment with an increase of about 6.4 (± 0.3)-fold. [score:2]
The inversely altered expression patterns of pro-apoptotic proteins Bax/Bak compared to the anti-apoptotic proteins Bcl2 and Bcl-xL, concordant with the elevated cytoplasmic cytochrome c levels and early breakdown of mitochondrial membrane potential, suggest for the involvement of mitochondrial apoptosis signaling in response to miR-147b-5p, miR-1912-5p, miR-96-5p and miR-3073a-3p resulting in the activation of caspase-3 and -7 and inactivation of PARP. [score:2]
MiR-1912 might overcome these resistance mechanisms by p53 independent mode of action and might open a novel therapeutic option in regard to potential targeted treatment of frequent recurrent platinum-resistant ovarian cancer [58]. [score:2]
However, hsa-miR-1912-5p and-3p showed decreased expression (0.5-fold) and miR-147b abundance was even further decreased (0.2-fold) compared to SGBS cells (Figure 5A). [score:2]
Hence, we selected the pro-apoptotic miR-147b-5p and miR-1912-5p showing a strong apoptosis induction in S KOV3 cells in addition to one mouse specific miRNA (miR-3073a-3p) showing pro-apoptotic effects in HCT 116 and S KOV3 cells. [score:1]
In order to substantiate our observations on pro-apoptotic effects of miR-1912-5p, miR-147b-5p, miR-96-5p and miR-3073a-3p in ovarian cell lines and to provide a better understanding of the underlying molecular mechanisms of action, further ovarian cancer cell lines with different genetic backgrounds were tested. [score:1]
A strong increase in the amount of cells with low ΔΨm in the presence of miRNA mimics was detectable within 48 h post transfection (S KOV3, miR-147b-5p, 54.0% ± 3.0% followed by almost comparable effects of miR-3073a-5p, 48.7% ± 3.2%, miR-96-5p, 47.4% ± 1.4% and miR-1912-5p, 40.0% ± 2.1%; Figure 6C). [score:1]
MiR- 147b-5p and miR-1912-5p showed significant pro-apoptotic effects in ovarian S KOV3p53null cells. [score:1]
30.5% ± 1.3%), with a slightly stronger effect of miR-1912-5p in both cell lines. [score:1]
These data support our previous findings that miR-3073a, miR-1912 and miR-147b seem to be involved in the progress of apoptosis in ovarian carcinoma cells and induce molecular changes including proteins of the intrinsic pathway as well as downstream effectors of apoptosis. [score:1]
In order to analyze potential synergistic effects with drugs already in use for ovarian cancer treatment, we analyzed apoptosis induction by carboplatin in combination with miR-1912-5p, -147b-5p, -96-5p or -3073a-3p in the established ovarian cancer cell line panel. [score:1]
miR-1912-5p, miR-147b-5p, miR-96-5p and miR-3073a-3p mediate pro-apoptotic effects in various ovarian cancer cell lines. [score:1]
Surprisingly only a few miRNAs including miR-1912-5p, -147b-5p, -682 and -93-3p were identified to induce apoptosis specifically in S KOV3 cells. [score:1]
While 5.5 μM carboplatin in combination with NT resulted in 26.7% (± 0.5%) apoptosis the number of cells in subG0/G1 was almost doubled to 55.0% (± 0.8%) by the addition of 50 nM miR-1912-5p. [score:1]
In case of A2780-cis the strongest increase was mediated by miR-1912-5p. [score:1]
Interestingly, apoptosis induction by miR-1912-5p and miR-147b-5p in cisplatin resistant A2780-cis cells (40.1% ± 1.9% vs. [score:1]
Analyzing the downstream effectors of apoptosis, we observed a three-fold increase of cleavaged caspase-3 (p17/p19) abundance and a moderate decrease in procaspase-3 for miR-96, miR-1912 and miR-3073a, while miR-147b even induced a sevenfold increase in caspase-3. Transient introduction of all four miRNA mimics individually induced moderate activation of PARP cleavage between 1.2 to 1.7-fold (Figure 6B). [score:1]
Based on these data, we further focused on the effects of the potentially S KOV3 specific miR-1912-5p and miR-147b-5p. [score:1]
S KOV3 cells were transiently transfected with all above analyzed miRNAs (miR-96-5p, miR-147b-5p, miR-1912-5p and miR-3073a-3p), harvested 72 h post transfection and subjected to immunoblotting. [score:1]
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2
[+] score: 3
Further, we also noticed altered expression of several miRNAs that were previously not reported including newly identified miRNAs such as miR-1178, miR-1261, miR-1912 and miR-2054, etc. [score:3]
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3
[+] score: 3
Genomic mapping of HTR2C transcripts (NM_000868, NM_001256760 and NM_001256761) and their six intragenic miRNAs (miR-1912, miR-764, miR-1264, miR-1298, miR-1911 and miR-488) as well as the expression correlation between HTR2C and these miRNAs. [score:3]
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4
[+] score: 3
According to our results, we hypothesized that circRNA_001059 may act as an inhibitor of miRNA by binding several specific miRNAs, including miR-30c-1*, miR-30c-2*, miR-122*, miR-139-3p, miR-339-5p and miR-1912. [score:3]
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5
[+] score: 1
Only one of those, mir-1912, matches a predicted microRNA gene found in our list (chrX:113792287-113792343:+) and this RNA was found to be enriched by Ago2 IP (File S2). [score:1]
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6
[+] score: 1
Other miRNAs from this paper: hsa-mir-15b, hsa-mir-608, hsa-mir-623, hsa-mir-1911
As seen in Fig S1 and Table S1, 11 out of 17 miRNA candidates were clearly positive on northern blots, suggesting that at least 11 novel miRNAs were identified; however, after the initial screen candidate 112 (miR-1911) has been included in the miRBase in addition to one of our un-validated candidates (candidate 111, miR-1912). [score:1]
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